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Ventricular Septal Defects in Adults

Naser M. Ammash, MD; and Carole A. Warnes, MD
[+] Article and Author Information

From the Mayo Clinic and Mayo Foundation, Rochester, Minnesota.


Acknowledgment: The authors thank Becky Hendrickson for technical support.

Requests for Single Reprints: Naser M. Ammash, MD, Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905.

Current Author Addresses: Drs. Ammash and Warnes: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905.


Ann Intern Med. 2001;135(9):812-824. doi:10.7326/0003-4819-135-9-200111060-00011
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Because congenital ventricular septal defects are of different sizes and locations, their clinical presentation, natural history, and treatment vary greatly. This review discusses the different types of ventricular septal defects commonly seen in adults in the authors' experience and in published literature. Ventricular septal defects are either isolated small defects or larger defects associated with pulmonary stenosis, pulmonary hypertension, or aortic regurgitation. These associations play an important role in the pathophysiologic consequences of the defect, its long-term complications, and treatment options. Knowledge of the different clinical presentations in adulthood and the specific features pertinent to these defects will help in the assessment and the care of adult patients with one of the most common congenital cardiac malformations.

Figures

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Figure 1.
Septal defects.

Top. Positions of different ventricular septal defects. 1 = membranous; 2 = subarterial or supracristal; 3 = muscular or trabecular; 4 = inlet or canal. (Modified from Capelli and colleagues [14] with permission of Excerpta Medica.) Bottom left. Membranous ventricular septal defect (VSD), as seen from the left ventricle, partially obliterated by the septal leaflet of the tricuspid valve (SLTV). Bottom right. Muscular VSD as seen from the left ventricle. (Photographs courtesy of Dr. William D. Edwards, Division of Anatomic Pathology, Mayo Clinic Rochester.)

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Figure 2.
Pathophysiology of aortic regurgitation.

In early systole (left), ejected blood from the left ventricle (LV) will be shunted through the ventricular septal defect. As a result, the anatomically unsupported coronary cusp and aortic sinus are driven into the right ventricle (RV) (middle); this is known as the Venturi effect. In diastole (right), the intra-aortic pressure forces the aortic valve leaflet to close, but the unsupported cusp (right or noncoronary) is pushed down into the left ventricular outflow tract away from the opposed coronary cusp, resulting in regurgitation. AR = aortic regurgitation; IVS = interventricular septum; PA = pulmonary artery. (Reproduced from Tatsuno and colleagues [23] with permission of the American Heart Association.)

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Figure 3.
The cardiac examination in ventricular septal defect (VSD).

Top left. Holosystolic murmur of VSD. Top middle. Shortened systolic murmur of muscular VSD. Top right. Typical murmur of VSD with mild pulmonary stenosis (PS) showing the delayed pulmonary closure sound (P2). Bottom left. Systolic ejection murmur of severe pulmonary stenosis with delayed and reduced P2. Bottom middle. Eisenmenger complex with absence of the holosystolic murmur of VSD, a loud P2 secondary to pulmonary hypertension, and pulmonary regurgitation (PR) diastolic murmur. Bottom right. VSD murmur followed by diastolic murmur of aortic regurgitation (AR); A2 = aortic closure sound; C = ejection click; S1 = first heart sound.

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Figure 4.
Electrocardiogram of a 42-year-old woman with Eisenmenger complex, demonstrating atrial fibrillation with right axis deviation, right ventricular hypertrophy, right bundle-branch block, and premature ventricular beat.
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Figure 5.
Chest radiograph in a patient with the Eisenmenger complex, showing cardiomegaly with severe enlargement of the proximal pulmonary arteries and pruning of the outer pulmonary vessels.
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Figure 6.
Echocardiographic examination of ventricular septal defects (VSDs).

Top left. Standard parasternal long-axis echocardiographic views show the membranous septum (MS), the infundibular septum (IS), and the trabecular muscular septum (TS). (Reproduced from Hagler and colleagues [13] with permission of the Mayo Foundation). Top right. Color-flow Doppler echocardiogram demonstrating a membranous VSD with a left-to-right shunt (red flow from left ventricle to right ventricle). Bottom left. Parasternal short-axis view. The asterisk indicates supracristal or subarterial ventricular septal defect in the right ventricular outflow tract. In the same basal view, the † indicates membranous ventricular septal defect in proximity to the tricuspid valve. Bottom right. Freeze-frame image of a membranous VSD (arrow), as seen on parasternal short-axis view. AO = aorta; AVS = atrioventricular septum; L = left coronary cusp; LA = left atrium; P = posterior noncoronary cusp; PA = pulmonary artery; R = right coronary cusp; RA = right atrium; RV = right ventricle.

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Figure 7.
Kaplan–Meier survival curve of all patients with ventricular septal defects (n= 1252) from the Natural History Study (dashed line) compared with the expected survival curve (solid line) for a sex- and age-matched population.

The number in parentheses indicates the number of patients remaining under observation 25 years after admission. (Reproduced from Kidd and colleagues [28] with permission of the American Heart Association.)

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Figure 8.
Survival rate for patients with ventricular septal defects by pulmonary artery systolic pressure.

The solid line indicates a pressure less than 50 mm Hg (n = 36); the dashed line indicates a pressure of 50 mm Hg or greater (n = 17). (Reproduced from Ellis and colleagues [25] with permission of the CV Mosby Company.)

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